Role of neutrophils in experimental septicemia and septic arthritis induced by Staphylococcus aureus

Verdrengh, Margareta; Tarkowski, Andrzej

doi:10.1128/iai.65.7.2517-2521.1997

Cited by 225 publications

(95 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The ease with which conditional lineage ablation strategies can be applied to the zebrafish (Davison et al, 2007) suggests that this will be a valuable organism for these studies. Both neutrophils and macrophages appear to be important in mammals: neutropenic mice are highly susceptible to S. aureus infection in septic arthritis models, with S. aureus present in the bloodstream of neutrophil-depleted mice but not wild-type controls (Verdrengh and Tarkowski, 1997). Similarly, monocyte/macrophage-depleted mice are also more susceptible to S. aureus, giving higher bacterial numbers in blood than in control animals (Verdrengh and Tarkowski, 2000).…”

Section: Discussionmentioning

confidence: 99%

A novel vertebrate model ofStaphylococcus aureusinfection reveals phagocyte-dependent resistance of zebrafish to non-host specialized pathogens

Prajsnar¹,

Cunliffe²,

Foster

et al. 2008

Cellular Microbiology

174

200

View full text Add to dashboard Cite

SummaryWith the emergence of multiply resistant Staphylococcus aureus, there is an urgent need to better understand the molecular determinants of S. aureus pathogenesis. A model of staphylococcal pathogenesis in zebrafish embryos has been established, in which host phagocytes are able to mount an effective immune response, preventing overwhelming infection from small inocula. Myeloid cell depletion, by pu.1 morpholino-modified antisense injection, removes this immune protection. Macrophages and neutrophils are both implicated in this immune response, phagocytosing circulating bacteria. In addition, in vivo phagocyte/bacteria interactions can be visualized within transparent embryos. A preliminary screen for bacterial pathogenesis determinants has shown that strains bearing mutations in perR, pheP and saeR are attenuated. perR and pheP mutants are deficient in growth in vivo, and their virulence is not fully restored by myeloid cell depletion. On the other hand, saeR mutants are able to grow in vivo, and are completely restored to virulence by myeloid cell depletion. Thus specific pathogen gene function can be matched with particular facets of host response. Zebrafish are a new addition to the tools available for the study of S. aureus pathogenesis, and may provide insights into the interactions of bacterial and host genomes in determining the outcome of infection.

show abstract

Section: Discussionmentioning

confidence: 99%

A novel vertebrate model ofStaphylococcus aureusinfection reveals phagocyte-dependent resistance of zebrafish to non-host specialized pathogens

Prajsnar¹,

Cunliffe²,

Foster

et al. 2008

Cellular Microbiology

174

200

View full text Add to dashboard Cite

show abstract

“…Adaptive immune response is required for an efficient containment of S. aureus during a persistent infection We (von Köckritz-Blickwede et al, 2008) and others (Mölne et al, 2000;Verdrengh & Tarkowski, 1997) have shown that neutrophil recruitment is critical for effective control of bacterial growth during the acute phase of S. aureus infection. To determine their relevance for bacterial containment during the persistent phase, we depleted neutrophils in S. aureus-infected mice at day 28 p.i.…”

Section: Research Articlementioning

confidence: 99%

The dynamics of T cells during persistent Staphylococcus aureus infection: from antigen‐reactivity to in vivo anergy

et al. 2011

View full text Add to dashboard Cite

Staphylococcus aureus is an important human pathogen that can cause long-lasting persistent infections. The mechanisms by which persistent infections are maintained involve both bacterial escape strategies and modulation of the host immune response. So far, the investigations in this area have focused on strategies used by S. aureus to persist within the host. Here, we used an experimental mouse model to investigate the host response to persistent S. aureus infection. Our results demonstrated that T cells, which are critical for controlling S. aureus infection, gradually lost their ability to respond to antigenic stimulation and entered a state of anergy with the progression of infection towards persistence. The T cell hyporesponsiveness was reverted by co-stimulation with the phorbol ester PMA, an activator of protein kinase C, suggesting that a failure in the T cell receptor (TCR)-proximal signalling events underlie the hyporesponsive phenotype. The presence of these anergic antigen-specific T cells may contribute to the failure of the host immune response to promote sterilizing immunity during persistent S. aureus infection and also offers new possibilities for novel immunotherapeutic approaches.

show abstract

“…Staphylococci and their products are capable of strongly inducing various cytokines and are capable of activating cellular immunity. Cytokines including interferon-g (IFN-g), interleukin-4 (IL-4), IL-10 and IL-18 reportedly regulate host resistance against S. aureus infection (Nakane et al, 1995;Verdrengh & Tarkowski, 1997;Sasaki et al, 2000;Gomez et al, 2002). IFN-g-deficient mice, IFN-g receptor-deficient mice and IL-4-deficient C57BL/6 mice increased survival rates of S. aureus infection compared with that of wild-type mice, whereas the development of septicemia by S. aureus infection was inhibited in IL-18-deficient mice Hultgren et al, 1999;Wei et al, 1999;Sasaki et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

The role of gamma interferon in acquired host resistance againstStaphylococcus aureusinfection in mice

Sasaki¹,

Tagawa²,

Iwakura³

et al. 2006

FEMS Immunology &Amp; Medical Microbiology

View full text Add to dashboard Cite

We investigated the expression of an acquired host resistance against Staphylococcus aureus infection in mice. When C57BL/6 mice were immunized with viable S. aureus and challenged with S. aureus eight weeks later, the elimination of S. aureus from the spleen and liver was enhanced in the immunized mice compared with the nonimmunized mice. When gamma interferon (IFN-gamma(-/-)) mice were immunized and challenged, the bacterial numbers in the organs of immunized mice were comparable to those in the nonimmunized mice, suggesting that IFN-gamma plays a critical role in an acquired host resistance against S. aureus infection. IFN-gamma(-/-) mice produced the lower level of anti-S. aureus immunoglobulin M (IgM) and IgG2a antibodies compared with C57BL/6 mice. To elucidate the role of IFN-gamma produced during a challenge with S. aureus, a single injection of anti-IFN-gamma monoclonal antibody to mice was carried out 1 h before challenge. An acquired resistance against S. aureus infection was inhibited by injecting with anti-IFN-gamma monoclonal antibody. However, anti-IFN-gamma monoclonal antibody treatment failed to modulate anti-S. aureus IgM, IgG1 or IgG2a responses in these animals. These results demonstrated that IFN-gamma is required for an acquired resistance against S. aureus infection in mice. However, IFN-gamma induced during the challenge failed to affect the secondary antibody responses.

show abstract

Role of neutrophils in experimental septicemia and septic arthritis induced by Staphylococcus aureus

Cited by 225 publications

References 28 publications

A novel vertebrate model ofStaphylococcus aureusinfection reveals phagocyte-dependent resistance of zebrafish to non-host specialized pathogens

A novel vertebrate model ofStaphylococcus aureusinfection reveals phagocyte-dependent resistance of zebrafish to non-host specialized pathogens

The dynamics of T cells during persistent Staphylococcus aureus infection: from antigen‐reactivity to in vivo anergy

The role of gamma interferon in acquired host resistance againstStaphylococcus aureusinfection in mice

Contact Info

Product

Resources

About